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Effects of transgene Oncostatin M on the development of retinal neuron in transgenic mice
1Department of Ophthalmology, Xiangya Hospital, Central South University, Changsha, 410008.
Purpose:
Oncostatin M (OSM) is a cytokine released by macrophages and lymphocytes that can function as a growth regulator. A current study shows that leukemia inhibitory factor (LIF), a homologue of OSM, can prevent photoreceptor cell death when expressed in the lens of transgenic mice. We determined the efforts of lens-specific overexpression of OSM on the development of eye.
Methods:
A truncated mouse OSM cDNA (-660 bp) was linked to the alpha A-crytallin promoter, and injected into single-cell embryos with microinjection. Then, transgenic mice were established. The mRNA expression of transgene OSM was detected by in situ hybridization. Immunohistochemistry was used to detect the expression of syntaxin, glial fibrillary acidic protein (GFAP), synaptophysin in the retinas of transgenic mice.
Results:
At embryonic day (E 17.5), the expression of the syntaxin at the inner and mid portion of the retinas of transgenic mice was much higher than that of the retinas of non-transgenic mice. The expression of GFAP was detected in the retinas of transgenic mice, while no expression in non-transgenic normal FVB (FVB/N) mice was detected in this stage. At postnatal day one (P1), the expression of synaptophysin was detected in the retinas of transgenic mice, but there was no such expression in FVB/N mice.
Conclusions:
Lens-specific overexpression of OSM induces premature differentiation of amacrine cells, gial cells, and photoreceptors in vivo.
Insights
Lens-specific overexpression of Oncostatin M (OSM) in mice induced premature differentiation of retinal cells, including amacrine cells, glial cells, and photoreceptors, impacting eye development.
Area of Science:
- Ophthalmology
- Developmental Biology
- Cell Biology
Background:
- Oncostatin M (OSM) is a cytokine with growth-regulating functions.
- Leukemia inhibitory factor (LIF), an OSM homologue, has shown potential in preventing photoreceptor cell death.
- The role of OSM in eye development requires further investigation.
Purpose of the Study:
- To investigate the effects of lens-specific overexpression of OSM on eye development.
- To determine if OSM can influence retinal cell differentiation and survival.
Main Methods:
- A truncated mouse OSM cDNA was linked to the alpha A-crystallin promoter.
- Transgenic mice were generated by microinjecting the construct into single-cell embryos.
- mRNA expression of OSM was analyzed using in situ hybridization.
- Immunohistochemistry was employed to detect syntaxin, GFAP, and synaptophysin expression in retinas.
Main Results:
- Syntaxin expression was significantly higher in the retinas of transgenic mice at embryonic day 17.5.
- Glial fibrillary acidic protein (GFAP) expression was detected in transgenic retinas but not in controls.
- Synaptophysin expression was observed in transgenic retinas at postnatal day one, unlike in controls.
Conclusions:
- Lens-specific overexpression of OSM leads to premature differentiation of amacrine cells, glial cells, and photoreceptors.
- OSM plays a role in regulating the differentiation of key retinal cell types during development.
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